The aim of this research is (1) to study reflex modulation of renin secretion and (2) to develop a model for central nervous hypertension. Our preliminary studies indicate that controlled respiratory acidosis increases renin activity while left atrial distension inhibits renin. Studies in these dogs will characterize the mechanisms whereby these reflexes modulate renal nerve activity and renin secretion. Attempts will be made to derive the relationships between renal nerve activity and renin secretion during such reflex adjustments.. In addition to reflex control of renin we will study acute and long-term effects of hypothalamic stimulation on renin control and blood pressure. The goal in these chronic beagles is to develop a model for central nervous hypertension and to study its etiology. The hypothesis in this model is that long-term intermittent stimulation of central nervous structures which activate renin release will lead to augmented angiotensin and increased sensitivity of vascular beds to catecholamines. Repeated stimulation during the period of increased sensitivity will yield greater vascular responses and further increments of renin. A positive feedback loop will have been initiated which will yield to hypertension. We will test this hypothesis by renin assay, renal sympathectomy adrenalectomy and a study of vascular sensitivity. The significance of this work lies in its potential for the study of reflex modulation of renin during normal and pathophysiologic states and for the potential development of a model for experimental hypertension.